Establishment and Multidimensional Pathological Evaluations of a Cigarette Smoke Exposure-Induced Chronic Obstructive Pulmonary Disease Mouse Model
10.12300/j.issn.1674-5817.2025.076
- VernacularTitle:香烟烟雾暴露诱导慢性阻塞性肺疾病小鼠模型的构建及多维度病理评估
- Author:
Jiaqi HE
1
;
Yuanyuan ZHOU
1
;
Yongqiang NIE
1
;
Zhaoxia WANG
1
;
Wangjie XU
1
Author Information
1. Laboratory Animal Center of Shanghai Jiao Tong University, Shanghai 200240, China
- Publication Type:Journal Article
- Keywords:
Chronic obstructive pulmonary disease;
Cigarette smoke exposure;
Mouse model;
Self-developed device;
Continuous exposure
- From:
Laboratory Animal and Comparative Medicine
2026;46(1):11-19
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo establish a reliable chronic obstructive pulmonary disease (COPD) mouse model based on a self-developed multichannel automatic control system for long-term continuous cigarette smoke exposure in small animals using a novel continuous cigarette smoke exposure method, and to conduct phenotypic evaluation and analysis, thereby providing an animal experimental basis for investigating COPD pathogenesis and prevention strategies. MethodsTwenty male C57BL/6J mice aged 6 weeks were randomly and equally divided into a control group and a model group. The model group (n=10) underwent 6 h of continuous cigarette smoke exposure daily (6 cigarettes per day for 12 consecutive weeks), while the control group (n=10) received no intervention. Body weight was monitored biweekly. Post-exposure, in vivo micro-CT imaging was performed. After euthanasia, serum and bronchoalveolar lavage fluid (BALF) levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were quantified by ELISA. Lung tissues underwent H&E and Masson's trichrome staining to observe changes in lung morphology and inflammatory cell infiltration, and the mean linear intercept (MLI) was calculated, thereby comprehensively evaluating the clinical features of COPD in the mouse model. ResultsCompared with the control group, the model group showed significantly reduced body weight (P<0.01) from the fourth week. Compared with the control group, IL-6 level in the serum and BALF of the model group increased by 27.2% and 140.0%, respectively (P<0.01). TNF-α level in the serum and bronchoalveolar lavage fluid of the model group increased by 16.7% (P<0.01) and 19.3% (P<0.05), respectively. Histopathological examination revealed alveolar wall thinning, septal rupture, emphysematous bullae formation, reduced alveolar count, bronchial wall thickening with lumen narrowing, and inflammatory cell infiltration. MLI was significantly elevated (P<0.01). Masson's staining confirmed collagen deposition and bronchial remodeling. Micro-CT demonstrated localized high-density shadows exhibiting typical features of chronic bronchitis. Conclusion The self-developed device enables long-term continuous smoke exposure, and the successfully established COPD mouse model exhibits pathological features highly consistent with clinical manifestations, offering an efficient and reliable tool for COPD research.
